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© Christine Schmitt, Anubis Vega Rua, Jean-Marc Panaud
Tête de moustique femelle Aedes albopictus, vecteur du virus de la dengue et du chikungunya. Microphotographie électronique à balayage, image colorisée.
Publication : Virology

Determinants in the envelope E protein and viral RNA helicase NS3 that influence the induction of apoptosis in response to infection with dengue type 1 virus

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Virology - 01 Sep 2000

Duarte dos Santos CN, Frenkiel MP, Courageot MP, Rocha CF, Vazeille-Falcoz MC, Wien MW, Rey FA, Deubel V, Desprès P

Link to Pubmed [PMID] – 10964773

Virology 2000 Sep;274(2):292-308

One mechanism by which dengue (DEN) virus may cause cell death is apoptosis. In this study, we investigated whether the genetic determinants responsible for acquisition by DEN type 1 (DEN-1) virus of mouse neurovirulence interfere with the induction of apoptosis. Neurovirulent variant FGA/NA d1d was generated during the adaptation of the human isolate of DEN-1 virus strain FGA/89 to grow in newborn mouse brains and mosquito cells in vitro [Desprès, P. Frenkiel, M. -P. Ceccaldi, P.-E. Duarte Dos Santos, C. and Deubel, V. (1998) J. Virol., 72: 823-829]. Genetic determinants possibly responsible for mouse neurovirulence were studied by sequencing the entire genomes of both DEN-1 viruses. Three amino acid differences in the envelope E protein and one in the nonstructural NS3 protein were found. The cytotoxicity of the mouse-neurovirulent DEN-1 variant was studied in different target cells in vitro and compared with the parental strain. FGA/NA d1d was more pathogenic for mouse neuroblastoma cells and attenuated for human hepatoma cells. Changes in virus replicative functions and virus assembly may account, in a large part, for the differences in the induction of apoptosis. Our data suggest that identified amino acid substitutions in the envelope E protein and viral RNA helicase NS3 may influence DEN-1 virus pathogenicity by altering viral growth.

http://www.ncbi.nlm.nih.gov/pubmed/10964773